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{{Redirect|Herpes|the virus that causes herpes simplex|Herpes simplex virus|all types of herpes viruses|Herpesviridae}}{{Infobox Disease |
Image = |
Caption = [[Electron Microscope|Electron micrograph]] of Herpes simplex virus. |
DiseasesDB = 5841 |
DiseasesDB_mult = {{DiseasesDB2|33021}} |
ICD10 = {{ICD10|A|60||a|50}}, {{ICD10|B|00||b|00}}, {{ICD10|G|05|1|g|00}}, {{ICD10|P|35|2|p|35}} |
ICD9 = {{ICD9|054.0}}, {{ICD9|054.1}}, {{ICD9|054.2}}, {{ICD9|054.3}}, {{ICD9|771.2}} |
ICDO = |
OMIM = |
MedlinePlus = |
eMedicineSubj = med |
eMedicineTopic = 1006 |
MeshID = D006561 }}


~~okay no problem
'''Herpes simplex''' ({{lang-grc|ἕρπης - herpes}}, lit. "creeping") is a [[viral disease]] caused by both herpes simplex virus 1 (HSV-1) and herpes simplex virus 2 (HSV-2). Infection with the herpes virus is categorized into one of several distinct disorders based on the site of infection. [[Herpes labialis|Oral herpes]], the visible symptoms of which are colloquially called ''cold sores'', infects the face and mouth. Oral herpes is the most common form of infection. [[Herpes genitalis|Genital herpes]], commonly known simply as ''herpes'', is the second most common form of herpes. Other disorders such as [[herpetic whitlow]], [[herpes gladiatorum]], ocular herpes ([[keratitis]]), cerebral herpes infection [[encephalitis]], [[Mollaret's meningitis]], [[Neonatal herpes simplex|neonatal herpes]], and possibly [[Bell's palsy]] are all caused by herpes simplex viruses.


wait a second wikipedia articles don't talk
Herpes viruses cycle between periods of active disease—presenting as blisters containing infectious [[virus]] particles—that last 2–21 days, followed by a [[remission (medicine)|remission]] period, during which the sores disappear. Genital herpes, however, is often [[asymptomatic]], though [[viral shedding]] may still occur. After initial infection, the viruses move to [[Sensory neuron|sensory nerves]], where they reside as life-long, [[Virus latency|latent]] viruses. Causes of recurrence are uncertain, though some potential triggers have been identified. Over time, episodes of active disease reduce in frequency and severity.


they do now
Herpes simplex is most easily transmitted by direct contact with a lesion or the body fluid of an infected individual. Transmission may also occur through skin-to-skin contact during periods of asymptomatic shedding. Barrier protection methods are the most reliable method of preventing transmission of herpes, but they merely reduce rather than eliminate risk. Oral herpes is easily diagnosed if the patient presents with visible sores or ulcers. Early stages of orofacial herpes and genital herpes are harder to diagnose; laboratory testing is usually required. Twenty percent of the U.S. population has antibodies to HSV-2, although not all of them have a history of genital lesions.<ref name="Harrison's">Harrison's Principles of Internal Medicine, 16th Ed., Ch. 163, Herpes simplex viruses, Lawrence Corey</ref>


okay
There is no cure for herpes. Once infected, the virus remains in the body for life. However, after several years, some people will become perpetually [[asymptomatic]] and will no longer experience outbreaks, though they may still be contagious to others. Vaccines are in [[clinical trials]] but have not demonstrated effectiveness. Treatments can reduce viral reproduction and shedding, prevent the virus from entering the skin, and alleviate the severity of symptomatic episodes.

Herpes simplex should not be confused with conditions caused by other viruses in the ''[[herpesviridae]]'' family such as [[herpes zoster]], which is a viral disease caused by [[varicella zoster virus]]. There is also a possibility of confusion with "hand, foot and mouth disease" due to apparition of lesions on the skin.


==Signs and Symptoms==
HSV infection causes several distinct medical [[Disorder (medicine)|disorders]]. Common infection of the skin or mucosa may affect the face and mouth (orofacial herpes), genitalia (genital herpes), or hands (herpes whitlow). More serious disorders occur when the virus infects and damages the eye (herpes keratitis), or invades the central nervous system, damaging the brain (herpes encephalitis). Patients with immature or suppressed immune systems, such as newborns, transplant recipients, or AIDS patients are prone to severe complications from HSV infections. HSV infection has also been associated with cognitive deficits of [[bipolar disorder]],<ref name="Dickerson2004 Mar 15">{{cite journal
|author=Dickerson FB, Boronow JJ, Stallings C, ''et al.'' |title=Infection with herpes simplex virus type 1 is associated with cognitive deficits in bipolar disorder |journal=Biol. Psychiatry |volume=55 |issue=6 |pages=588–93 |year=2004 |month=March |pmid=15013827 |doi=10.1016/j.biopsych.2003.10.008
}}</ref> and [[Alzheimer's disease]],<ref name="Itzhaki1997 Jan 25">{{cite journal
|author=Itzhaki RF, Lin WR, Shang D, Wilcock GK, Faragher B, Jamieson GA |title=Herpes simplex virus type 1 in brain and risk of Alzheimer's disease |journal=Lancet |volume=349 |issue=9047 |pages=241–4 |year=1997 |month=January |pmid=9014911 |doi=10.1016/S0140-6736(96)10149-5
}}</ref> although this is often dependent on the [[genetics]] of the infected person.

There is a single report of a [[systemic infection]] with HSV-2, where a healthy 28-year old woman with a healthy immune system died 12 days after contracting the virus.<ref name="Southern Medical Journal Jan 1983">{{cite journal|author=Whorton CM, Thomas DM, Denham SW|journal=Southern Medial Journal|pages=81–3|month=January|year=1983|volume=76(1)|pmid=6297097|title=Fatal systemic herpes simplex virus type 2 infection in a healthy young woman}}</ref>

In all cases HSV is never removed from the body by the [[immune system]]. Following a primary infection, the virus enters the nerves at the site of primary infection, migrates to the [[cell body]] of the neuron, and becomes latent in the [[ganglion]].<ref name="pmid18156035">{{cite journal |author=Gupta R, Warren T, Wald A |title=Genital herpes |journal=Lancet |volume=370 |issue=9605 |pages=2127–37 |year=2007 |month=December |pmid=18156035 |doi=10.1016/S0140-6736(07)61908-4 |url=http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(07)61908-4}}</ref> As a result of primary infection, the body produces antibodies to the particular type of HSV involved, preventing a subsequent infection of that type at a different site. In HSV-1 infected individuals, [[seroconversion]] after an oral infection will prevent additional HSV-1 infections such as whitlow, genital herpes, and keratitis. Prior HSV-1 seroconversion seems to reduce the symptoms of a later HSV-2 infection, although HSV-2 can still be contracted. Most indications are that an HSV-2 infection contracted prior to HSV-1 seroconversion will also immunize that person against HSV-1 infection.<ref name="Brown1997 Aug 21">{{cite journal
|author=Brown ZA, Selke S, Zeh J, ''et al.'' |title=The acquisition of herpes simplex virus during pregnancy |journal=N Engl J Med. |volume=337 |issue=8 |pages=509–15 |year=1997 |month=August |pmid=9262493
|url=http://content.nejm.org/cgi/content/full/337/8/509
|doi=10.1056/NEJM199708213370801
}}</ref>

{| class="wikitable"
|-
! Condition
! Description
! Illustration
|-
| [[Herpes labialis]]
| Infection occurs when the virus comes into contact with oral mucosa or abraded skin.
| [[Image:Cold sore.jpg|center|150px]]
|-
| [[Herpes genitalis]]
| When symptomatic, the typical manifestation of a primary HSV-1 or HSV-2 genital infection is clusters of inflamed [[papule]]s and [[Vesicle (dermatology)|vesicles]] on the outer surface of the genitals resembling cold sores.
| [[Image:SOA-Herpes-genitalis-female.jpg|center|150px]]
|-
| [[Herpetic whitlow]]
| Herpes whitlow is a painful infection that typically affects the fingers or thumbs. Occasionally infection occurs on the toes or on the nail cuticle.
|
|-
| [[Herpes gladiatorum]]
| Individuals that participate in [[contact sport]]s such as [[wrestling]], [[Rugby football|rugby]], and [[soccer]] sometimes acquire a condition caused by HSV-1 known as [[herpes gladiatorum]], ''scrumpox'', ''wrestler’s herpes'', or ''mat herpes'', which presents as skin ulceration on the face, ears, and neck. Symptoms include fever, headache, sore throat and swollen glands. It occasionally affects the eyes or eyelids.
|
|-
| [[Herpetic keratoconjunctivitis]]
| Primary infection typically presents as swelling of the [[conjunctiva]] and eye-lids ([[blepharoconjunctivitis]]), accompanied by small white itchy lesions on the surface of the [[cornea]].
|
|-
| [[Herpesviral encephalitis]]
| A herpetic infection of the brain that is thought to be caused by the [[Retrograde infection|retrograde transmission]] of virus from a peripheral site on the face following HSV-1 reactivation, along the [[trigeminal nerve]] [[axon]], to the brain. HSV is the most common cause of viral encephalitis. When infecting the brain, the virus shows a preference for the [[temporal lobe]].<ref>http://emedicine.medscape.com/article/341142-overview eMedicine</ref>.
| [[File:Hsv encephalitis.jpg|center|150px]]
|-
| [[Herpesviral meningitis]]
| HSV-2 is the most common cause of Mollaret's meningitis, a type of recurrent viral meningitis.
|
|-
| [[Neonatal herpes simplex]]
| [[Infant|Neonatal]] HSV infection is a rare but serious condition, usually caused by [[vertical transmission]] of HSV (type 1 or 2) from mother to newborn.
|
|-
|-
| During [[immunodeficiency]]
| In patients with a weakened immune system, herpes simplex can cause unusual lesions in the skin. One of the most striking is the appearance of clean linear erosions in skin creases, with the appearance of a knife cut.<ref>{{cite journal|title=Linear erosive Herpes Simplex Virus infection in immunocompromised patients: the “Knife-Cut Sign”|journal=Clin Infect Dis|year=2008|volume=47|pages=1440–1441|doi=10.1086/592976|author=Jocelyn A. Lieb, Stacey Brisman, Sara Herman, Jennifer MacGregor, Marc E. Grossman}}</ref>
|-
| [[Herpetic sycosis]]
| Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicle.<ref name="Andrews">{{cite book |author=James, William D.; Berger, Timothy G.; et al. |title=Andrews' Diseases of the Skin: clinical Dermatology |publisher=Saunders Elsevier |location= |year=2006 |pages= |isbn=0-7216-2921-0 |oclc= |doi= |accessdate=}}</ref>{{rp|369}}
|-
| [[Eczema herpeticum]]
| Infection with herpesvirus in patients with chronic [[atopic dermatitis]] may result in spread of herpes simples throughout the eczematous areas.<ref name="Andrews" />{{rp|373}}
|}

===Association with neuronal disorders===
====Bell's palsy====
In a mouse model, a type of facial [[paralysis]] called [[Bell's palsy]] has been linked to the presence and reactivation of latent HSV-1 inside the sensory nerves of the face ([[geniculate ganglion|geniculate ganglia]]).<ref name="pmid1336296">{{cite journal
|author=Takasu T, Furuta Y, Sato KC, Fukuda S, Inuyama Y, Nagashima K
|title=Detection of latent herpes simplex virus DNA and RNA in human geniculate ganglia by the polymerase chain reaction
|journal=Acta Otolaryngol. jhkbjk

|volume=112
|issue=6
|pages=1004–11
|year=1992
|pmid=1336296
|doi=10.3109/00016489209137502 }}</ref><ref name="pmid7598372">{{cite journal
|author=Sugita T, Murakami S, Yanagihara N, Fujiwara Y, Hirata Y, Kurata T
|title=Facial nerve paralysis induced by herpes simplex virus in mice: an animal model of acute and transient facial paralysis
|journal=Ann. Otol. Rhinol. Laryngol.
|volume=104
|issue=7
|pages=574–81
|year=1995
|pmid=7598372 }}</ref> This is supported by findings that show the presence of HSV-1 DNA in saliva at a higher frequency in patients with Bell's palsy relative to those without the condition.<ref name="pmid16917546">{{cite journal
|author=Lazarini PR, Vianna MF, Alcantara MP, Scalia RA, Caiaffa Filho HH
|title=Herpes simplex virus in the saliva of peripheral Bell's palsy patients
|language=Portuguese
|journal=Rev Bras Otorrinolaringol (Engl Ed)
|volume=72
|issue=1
|pages=7–11
|year=2006
|pmid=16917546 }}</ref>

However, since HSV can also be detected in these ganglia in large numbers of individuals that have never experienced facial paralysis, and high titers of antibodies for HSV are not found in HSV-infected individuals with Bell's palsy relative to those without, this theory has been contested.<ref name="pmid15699730">{{cite journal
|author=Linder T, Bossart W, Bodmer D
|title=Bell's palsy and Herpes simplex virus: fact or mystery?
|journal=Otol. Neurotol.
|volume=26
|issue=1
|pages=109–13
|year=2005
|pmid=15699730
|doi=10.1097/00129492-200501000-00020 }}</ref> In other studies, HSV-1 DNA was not detected in the [[cerebrospinal fluid]] of Bell's palsy sufferers, raising questions whether HSV-1 is the causative agent in this type of facial paralysis.<ref name="pmid17573575">{{cite journal
|author=Kanerva M, Mannonen L, Piiparinen H, Peltomaa M, Vaheri A, Pitkäranta A
|title=Search for Herpesviruses in cerebrospinal fluid of facial palsy patients by PCR
|journal=Acta Otolaryngol.
|volume=127
|issue=7
|pages=775–9
|year=2007
|pmid=17573575
|doi=10.1080/00016480601011444}}</ref><ref name="pmid16676828">{{cite journal
|author=Stjernquist-Desatnik A, Skoog E, Aurelius E
|title=Detection of herpes simplex and varicella-zoster viruses in patients with Bell's palsy by the polymerase chain reaction technique
|journal=Ann. Otol. Rhinol. Laryngol.
|volume=115
|issue=4
|pages=306–11
|year=2006
|pmid=16676828 }}</ref> The potential effect of HSV-1 in the etiology of Bell's palsy has prompted the use of antiviral medication to treat the condition. The benefits of acyclovir and valacyclovir have been studied.<ref name="pmid17956069">{{cite journal
|author=Tiemstra JD, Khatkhate N
|title=Bell's palsy: diagnosis and management
|journal=Am Fam Physician
|volume=76
|issue=7
|pages=997–1002
|year=2007
|pmid=17956069 }}</ref> But the effect appears small, if at all detectable.

====Alzheimer's disease====
Scientists discovered a link between HSV-1 and [[Alzheimer's disease]] in 1979.<ref>{{cite journal|author=Middleton PJ, Peteric M, Kozak M, Rewcastle NB, McLachlan DR. |title=Herpes simplex viral genome and senile and presenile dementias of Alzheimer and Pick. |journal=Lancet |year=1980 |volume= 315|issue= |page=1038 |doi=10.1016/S0140-6736(80)91490-7}}</ref> In the presence of a certain gene variation ([[Apolipoprotein E|APOE]]-epsilon4 allele carriers), HSV-1 appears to be particularly damaging to the nervous system and increases one’s risk of developing Alzheimer’s disease. The virus interacts with the components and receptors of [[lipoproteins]], which may lead to the development of Alzheimer's disease.<ref name="Dobson1999">{{cite journal
|author=Dobson CB, Itzhaki RF |title=Herpes simplex virus type 1 and Alzheimer's disease |journal=Neurobiol. Aging |volume=20 |issue=4 |pages=457–65 |year=1999 |pmid=10604441 |url=http://linkinghub.elsevier.com/retrieve/pii/S0197-4580(99)00055-X
|doi=10.1016/S0197-4580(99)00055-X
}}</ref><ref>This research identifies HSVs as the pathogen most clearly linked to the 2001{{cite journal
|author=Pyles RB |title=The association of herpes simplex virus and Alzheimer's disease: a potential synthesis of genetic and environmental factors |journal=Herpes |volume=8 |issue=3 |pages=64–8 |year=2001 |month=November |pmid=11867022
|url=http://www.ihmf.com/journal/download/83pyles(64)vol864.pdf
|format=PDF}}</ref> Without the presence of the gene allele, HSV type 1 does not appear to cause any neurological damage and thus increase the risk of Alzheimer’s.<ref name=Itzhaki1997>{{cite journal
|author=Itzhaki RF, Lin WR, Shang D, Wilcock GK, Faragher B, Jamieson GA |title=Herpes simplex virus type 1 in brain and risk of Alzheimer's disease |journal=Lancet |volume=349 |issue=9047 |pages=241–4 |year=1997 |month=January |pmid=9014911 |doi=10.1016/S0140-6736(96)10149-5 }}</ref>

A study published in ''The Journal of Pathology'',<ref name=Itzhaki2008>{{cite journal |author=Wozniak MA, Mee AP, Itzhaki RF |title=Herpes simplex virus type 1 DNA is located within Alzheimer's disease amyloid plaques |journal=J Pathol. |volume=217 |issue=1 |pages=131–8 |year=2009 |month=January |pmid=18973185 |doi=10.1002/path.2449 |url=http://www3.interscience.wiley.com/journal/121411445/abstract }}</ref> has shown a striking localization of herpes simplex virus type 1 DNA within the beta-amyloid plaques that characterize Alzheimer's disease. It suggests that this virus is a major cause of the plaques and hence probably a significant aetiological factor in Alzheimer's disease.

==Mechanism==
Herpes is contracted through direct contact with an active lesion or body fluid of an infected person.<ref name="titleAHMF: Preventing Sexual Transmission of Genital Herpes">{{cite web |url=http://www.ahmf.com.au/health_professionals/guidelines/preventing_gh_transmission.htm |title=AHMF: Preventing Sexual Transmission of Genital herpes |accessdate=2008-02-24 |work=}}</ref> Herpes transmission occurs between discordant partners; a person with a history of infection (HSV seropositive) can pass the virus to an HSV seronegative person. The only way to contract Herpes simplex virus 2 is through direct skin-to-skin contact with an infected individual.{{Citation needed|date=January 2010}} To infect a new individual, HSV travels through tiny breaks in the skin or mucous membranes in the mouth or genital areas. Even microscopic abrasions on mucous membranes are sufficient to allow viral entry.

HSV asymptomatic [[viral shedding|shedding]] occurs at some time in most individuals infected with herpes. It can occur more than a week before or after a symptomatic recurrence in 50% of cases.<ref name="pmid16238897"/> Infected people that show no visible symptoms may still shed and transmit virus through their skin; asymptomatic shedding may represent the most common form of HSV-2 transmission.<ref name="pmid16238897">{{cite journal |author=Leone P |title=Reducing the risk of transmitting genital herpes: advances in understanding and therapy |journal=Curr Med Res Opin |volume=21 |issue=10 |pages=1577–82 |year=2005 |pmid=16238897 |doi=10.1185/030079905X61901}}</ref> Asymptomatic shedding is more frequent within the first 12 months of acquiring HSV. Concurrent infection with [[Human Immunodeficiency Virus|HIV]] increases the frequency and duration of asymptomatic shedding.<ref>{{cite journal | author = Kim H, Meier A, Huang M, Kuntz S, Selke S, Celum C, Corey L, Wald A | title = Oral herpes simplex virus type 2 reactivation in HIV-positive and -negative men. | journal = J Infect Dis | volume = 194 | issue = 4 | pages = 420–7 | year = 2006 | pmid = 16845624 | doi = 10.1086/505879}}</ref> There are indications that some individuals may have much lower patterns of shedding, but evidence supporting this is not fully verified; no significant differences are seen in the frequency of asymptomatic shedding when comparing persons with one to twelve annual recurrences to those who have no recurrences.<ref name="pmid16238897"/>

Antibodies that develop following an initial infection with a type of HSV prevents reinfection with the same virus type—a person with a history of orofacial infection caused by HSV-1 cannot contract herpes whitlow or a genital infection caused by HSV-1. In a [[monogamy|monogamous]] couple, a seronegative female runs a greater than 30% per year risk of contracting an HSV infection from a seropositive male partner.<ref name=Mertz1993>{{cite journal
| author = Mertz, G.J.
| year = 1993
| title = Epidemiology of genital herpes infections.
| journal = Infect Dis Clin North Am
| volume = 7
| issue = 4
| pages = 825–39
| pmid = 8106731}}</ref> If an oral HSV-1 infection is contracted first, seroconversion will have occurred after 6 weeks to provide protective antibodies against a future genital HSV-1 infection.

==Diagnosis==
Primary orofacial herpes is readily identified by clinical examination of persons with no previous history of lesions and contact with an individual with known HSV-1 infection. The appearance and distribution of sores in these individuals typically presents as multiple, round, superficial oral ulcers, accompanied by acute [[gingivitis]].<ref name="pmid17939933">{{cite journal |author=Fatahzadeh M, Schwartz RA |title=Human herpes simplex virus infections: epidemiology, pathogenesis, symptomatology, diagnosis, and management |journal=J. Am. Acad. Dermatol. |volume=57 |issue=5 |pages=737–63; quiz 764–6 |year=2007 |pmid=17939933 |doi=10.1016/j.jaad.2007.06.027}}</ref> Adults with non-typical presentation are more difficult to diagnose. Prodromal symptoms that occur before the appearance of herpetic lesions help differentiate HSV symptoms from the similar symptoms of other disorders, such as [[allergy|allergic]] [[stomatitis]]. When lesions do not appear inside the mouth, primary orofacial herpes is sometimes mistaken for [[impetigo]], a bacterial [[infection]]. Common mouth ulcers ([[aphthous ulcer]]) also resemble intraoral herpes, but do not present a [[Vesicle (dermatology)|vesicular]] stage.<ref name="pmid17939933"/>

Genital herpes can be more difficult to diagnose than oral herpes since most HSV-2-infected persons have no classical symptoms.<ref name="pmid17939933"/> Further confusing diagnosis, several other conditions resemble genital herpes, including [[lichen planus]], [[atopic dermatitis]], and [[urethritis]].<ref name="pmid17939933"/> [[Laboratory]] testing is often used to confirm a diagnosis of genital herpes. Laboratory tests include: culture of the virus, [[direct fluorescent antibody]] (DFA) studies to detect virus, [[skin biopsy]], and [[polymerase chain reaction]] (PCR) to test for presence of viral DNA. Although these procedures produce highly sensitive and specific diagnoses, their high costs and time constraints discourage their regular use in clinical practice.<ref name="pmid17939933"/>

[[Serology|Serological]] tests for antibodies to HSV are rarely useful to diagnosis and not routinely used in clinical practice<ref name="pmid17939933"/>, but are important in epidemiological studies. Serologic assays cannot differentiate between antibodies generated in response to a genital versus or an oral HSV infection, and as such cannot confirm the site of infection. Absence of antibody to HSV-2 does not exclude genital infection, because of the increasing incidence of genital infections caused by HSV-1.

==Prevention==
[[Image:Kondom.jpg|thumb|Barrier protection, such as a [[condom]], can reduce the risk of herpes transmission.]]

[[Condom]]s offer moderate protection against HSV-2 in both men and women, with consistent condom users having a 30% lower risk of HSV-2 acquisition compared with those who never use condoms<ref name=Martin>{{cite journal | author=Emily T. Martin, MPH; Elizabeth Krantz, MS; Sami L. Gottlieb, MD, MSPH; Amalia S. Magaret, PhD; Andria Langenberg, MD; Lawrence Stanberry, MD, PhD; Mary Kamb, MD, MPH; Anna Wald, MD, MPH | title=A Pooled Analysis of the Effect of Condoms in Preventing HSV-2 Acquisition | journal=Archives of Internal Medicine | year=2009 | pages=1233-1240 | volume=169 | issue=13 | pmid= | url=http://archinte.ama-assn.org/cgi/content/abstract/169/13/1233 | doi=}}</ref> The virus cannot pass through a latex condom, but a condom's effectiveness is limited because it does not prevent skin contact or bodily fluid contact with the scrotum, anus, buttocks, upper thighs or area immediately surrounding the penis, all of which are susceptible to infection with and transmission of the virus. Preventing contact with these areas during sex, in addition to wearing a condom, should theoretically provide enhanced protection against herpes. Wearing clothing or [[undergarments]] such as [[boxer shorts]] that cover these susceptible areas but still allow access to the genitals through a small opening (such as a fly) should help prevent transmission and infection.

The use of condoms or [[dental dams]] also limits the transmission of herpes from the genitals of one partner to the mouth of the other (or vice versa) during [[oral sex]]. When one partner has a herpes simplex infection and the other does not, the use of antiviral medication, such as [[valaciclovir]], in conjunction with a condom, further decreases the chances of transmission to the uninfected partner.<ref name="pmid18156035"/> Topical [[microbicide]]s which contain chemicals that directly inactivate the virus and block viral entry are being investigated.<ref name="pmid18156035"/> [[Vaccines]] for HSV are undergoing trials. Once developed, they may be used to help with prevention or minimize initial infections as well as treatment for existing infections.<ref>{{cite news | last =Seppa | first =Nathan | title =One-Two Punch: Vaccine fights herpes with antibodies, T cells | page =5 | publisher =Science News | date= 2005-01-05 | url =http://www.sciencenews.org/articles/20050101/fob6.asp | accessdate = 2007-03-29}}</ref>

As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men.<ref> {{cite news | author=Carla K. Johnson | title=Percentage of people with herpes drops | url=http://www.newsobserver.com/150/story/477928.html | publisher=Associated Press | date= August 23, 2006}}</ref> On an annual basis, without the use of antivirals or condoms, the transmission risk of HSV-2 from infected male to female is approximately 8-10%.<ref name=Mertz1993>{{cite journal
|author=Mertz GJ |title=Epidemiology of genital herpes infections |journal=Infect Dis Clin North Am. |volume=7 |issue=4 |pages=825–39 |year=1993 |month=December |pmid=8106731
}}</ref><ref name=Kulhanjian1992>{{cite journal
|author=Kulhanjian JA, Soroush V, Au DS, ''et al.'' |title=Identification of women at unsuspected risk of primary infection with herpes simplex virus type 2 during pregnancy |journal=N. Engl. J. Med. |volume=326 |issue=14 |pages=916–20 |pmid=1311799 |url=http://content.nejm.org/cgi/content/abstract/326/14/916
|date= April 2, 1992 }}</ref>
This is believed to be due to the increased exposure of mucosal tissue to potential infection sites. Transmission risk from infected female to male is approximately 4-5% annually.<ref name=Kulhanjian1992/> Suppressive antiviral therapy reduces these risks by 50%.<ref name=Corey2004>{{cite journal
|author=Corey L, Wald A, Patel R, ''et al.'' |title=Once-daily valacyclovir to reduce the risk of transmission of genital herpes |journal=N Engl J Med. |volume=350 |issue=1 |pages=11–20 |year=2004 |month=January |pmid=14702423 |doi=10.1056/NEJMoa035144 |url=http://content.nejm.org/cgi/reprint/350/1/11.pdf
|format=PDF}}</ref> Antivirals also help prevent the development of symptomatic HSV in infection scenarios—meaning the infected partner will be seropositive but symptom free—by about 50%. Condom use also reduces the transmission risk by 50%.<ref name=Wald>{{cite journal | author=Wald A, Langenberg AG, Link K, Izu AE, Ashley R, Warren T, Tyring S, Douglas JM Jr, Corey L. | title=Effect of condoms on reducing the transmission of herpes simplex virus type 2 from men to women | journal=JAMA | year=2001 | pages=3100–3106 | volume=285 | issue=24 | pmid=11427138 | url=http://jama.ama-assn.org/cgi/content/full/285/24/3100 | doi=10.1001/jama.285.24.3100}}</ref><ref name=Casper>{{cite journal | author=Casper C, Wald A. | title=Condom use and the prevention of genital herpes acquisition, | journal=Herpes | year=2002 | pages=10–14 | volume=9 | issue=1 | pmid=11916494 | url=http://www.ihmf.org/journal/download/91casper(10)vol910.pdf|format=PDF}}</ref><ref name=Wald2005>{{cite journal
|author=Wald A, Langenberg AG, Krantz E, ''et al.'' |title=The relationship between condom use and herpes simplex virus acquisition |journal=Ann Intern Med. |volume=143 |issue=10 |pages=707–13 |year=2005 |month=November |pmid=16287791 |url=http://www.annals.org/cgi/reprint/143/10/707
}}</ref> Condom use is much more effective at preventing male to female transmission than vice-versa.<ref name=Wald/> The effects of combining antiviral and condom use is roughly additive, thus resulting in approximately a 75% combined reduction in annual transmission risk.{{Citation needed|date=May 2008}} These figures reflect experiences with subjects having frequently ecurring genital herpes (>6 recurrences per year). Subjects with low recurrence rates and those with no clinical manifestations were excluded from these studies.{{Citation needed|date=May 2008}}

The risk of transmission from mother to baby is highest if the mother becomes infected at around the time of delivery (transmission risk 30 to 60%),<ref>{{cit journal|author=Brown ZA, Selke S, Zeh J ''et al.''|title=The acquisition of herpes simplex virus during pregnancy|journal=N Engl J Med|volume=337|pages=509&ndash;515|year=1997}}</ref><ref>{{cite journal|author=Brown ZA, Wald A, Morrow RA, Selke S, Zeh J, Corey L|title=Effect of serologic status and cesarean delivery on transmission rates of herpes simplex virus from mother to infant|journal=JAMA|volume=289|pages=203&ndash;209|year=2003|doi=10.1001/jama.289.2.203|pmid=12517231}}</ref> but the risk falls to 3% if it is a recurrent infection, and is less than 1% if there are no visible lesions.<ref>{{cite journal|author=Brown ZA, Benedetti J, Ashley R ''et al.''|title=Neonatal herpes simplex virus infection in relation to asymptomatic maternal infection at the time of labor|journal=N Engl J Med|volume=324|page=1247|year=1991}}</ref> To prevent neonatal infections, seronegative women are recommended to avoid unprotected oral-genital contact with an HSV-1 seropositive partner and conventional sex with a partner having a genital infection during the last trimester of pregnancy. A seronegative mother that contracts HSV at this time has up to a 57% chance of conveying the infection to her baby during childbirth, since insufficient time will have occurred for the generation and transfer of protective maternal antibodies before the birth of the child, whereas a woman seropositive for both HSV-1 and HSV-2 has around a 1-3% chance of transmitting infection to her infant.
HSV-1 being transmitted by oral sex as HSV-2 is not very common but there is always the risk <ref name=Whitley_RJ>{{cite journal
| author= Whitley RJ, Kimberlin DW, Roizman B
| title=Herpes simplex viruses
| journal=Clin Infect Dis
| year=1998
| pages=541–53
| volume=26
| issue=3
| pmid=9524821
|doi= 10.1086/514600|url=http://www.journals.uchicago.edu/doi/pdf/10.1086/514600
}}</ref><ref name="pmid1849612">{{cite journal |author=Brown ZA, Benedetti J, Ashley R, ''et al.'' |title=Neonatal herpes simplex virus infection in relation to asymptomatic maternal infection at the time of labor |journal=N. Engl. J. Med. |volume=324 |issue=18 |pages=1247–52 |year=1991 |month=May |pmid=1849612 |doi= |url=}}</ref> Women that are seropositive for only one type of HSV are only half as likely to transmit HSV as infected seronegative mothers. Mothers infected with HSV are advised to avoid procedures that would cause trauma to the infant during birth (e.g., fetal scalp electrodes, forceps, and vacuum extractors) and, should lesions be present, to elect [[caesarean section]] to reduce exposure of the child to infected secretions in the birth canal.<ref name="pmid18156035"/> The use of antiviral treatments, such as acyclovir, given from the 36th week of pregnancy, limits HSV recurrence and shedding during childbirth, thereby reducing the need for caesarean section.<ref name="pmid18156035"/>

HSV-2 infected individuals are at higher risk for acquiring [[HIV]] when practicing unprotected sex with HIV-positive persons,<ref>{{cite journal
|author=Sobngwi‐Tambekou J, Taljaard D, Lissouba P, ''et al.''
|title=Effect of HSV‐2 Serostatus on Acquisition of HIV by Young Men: Results of a Longitudinal Study in Orange Farm, South Africa
|journal=J Infect Dis
|volume=199
|pages=958&ndash;964
|doi=10.1086/597208
|year=2009}}</ref> particularly during an outbreak with active lesions.<ref name="pmid18186706">{{cite journal |author=Koelle DM, Corey L |title=Herpes Simplex: Insights on Pathogenesis and Possible Vaccines |journal=Annu Rev Med |volume=59 |issue= |pages=381&ndash;395 |year=2008 |pmid=18186706 |doi=10.1146/annurev.med.59.061606.095540}}</ref>

==Treatment==
There is no cure that can eradicate herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. Antiviral drugs also reduce asymptomatic shedding; it is believed asymptomatic Genital HSV-2 viral shedding occurs on 20% of days per year in patients not undergoing antiviral treatment, versus 10% of days while on antiviral therapy.<ref name="pmid16238897"/> Non-prescription [[analgesic]]s can reduce pain and fever during initial outbreaks. Topical anesthetic treatments such as [[prilocaine]], [[lidocaine]] or [[tetracaine]] can also relieve itching and pain.<ref name="pmid3147021">{{cite journal
|author=
|title=Local anesthetic creams
|journal=BMJ
|volume=297
|issue=6661
|page=1468
|year=1988
|pmid=3147021
|doi=}}</ref><ref name="pmid10570387">{{cite journal
|author=Kaminester LH, Pariser RJ, Pariser DM, ''et al.''
|title=A double-blind, placebo-controlled study of topical tetracaine in the treatment of herpes labialis
|journal=J. Am. Acad. Derm
|volume=41
|issue=6
|pages=996–1001
|year=1999
|pmid=10570387
|doi=10.1016/S0190-9622(99)70260-4 }}</ref>

===Antiviral medication===
[[Image:Acyclovir pills.jpg|thumb|The antiviral medication acyclovir]]

[[Antiviral drug|Antiviral medications]] used against herpes viruses work by interfering with [[viral replication]], effectively slowing the replication rate of the virus and providing a greater opportunity for the immune response to intervene. All drugs in this class depend on the activity of the viral [[enzyme]] [[thymidine kinase]] to convert the drug sequentially from its [[prodrug]] form to monophosphate (with one [[phosphate]] group), diphosphate (with two phosphate groups), and finally to the triphosphate (with three phosphate groups) form which interferes with viral [[DNA replication]].<ref name="pmid16284630">{{cite journal
|author=De Clercq E, Field HJ
|title=Antiviral prodrugs - the development of successful prodrug strategies for antiviral chemotherapy
|journal=Br. J. Pharmacol.
|volume=147
|issue=1
|pages=1–11
|year=2006
|pmid=16284630
|doi=10.1038/sj.bjp.0706446}}</ref>

There are several prescription [[Antiviral drug|antiviral]] medications for controlling herpes simplex outbreaks, such as [[aciclovir]] (Zovirax), [[valaciclovir]] (Valtrex), [[famciclovir]] (Famvir), and [[penciclovir]]. Acyclovir was the original, and prototypical, member of this drug class; it is now available in generic brands at a greatly reduced cost. Valaciclovir and famciclovir—prodrugs of aciclovir and penciclovir, respectively—have improved solubility in water and better [[bioavailability]] when taken orally.<ref name="pmid16284630"/> Aciclovir is the recommended antiviral for suppressive therapy for use during the last months of pregnancy to prevent transmission of herpes simplex to the [[neonate]] in cases of maternal recurrent herpes. Benzocaine is a substance in most nonprescription drug medications that can treat cold sores and reduce the severity of the symptoms.<ref name="Leung">{{cite journal
| author=Leung DT, Sacks SL.
| title=Current treatment options to prevent perinatal transmission of herpes simplex virus
| journal=Expert Opin. Pharmacother.
| year=2003
| pages=1809–1819
| volume=4
| issue=10
| pmid=14521490
| doi=10.1517/14656566.4.10.1809}}</ref>
The use of valaciclovir and famciclovir, while potentially improving treatment compliance and efficacy, are still undergoing safety evaluation in this context.

Several studies in humans and mice provide evidence that early treatment with famciclovir soon after the first infection with herpes can significantly lower the chance of future outbreaks of herpes. Early use of famciclovir has been shown to reduce the amount of latent virus in the neural ganglia.<ref>The effects of antiviral therapy on the distribution of herpes simplex virus type 1 to ganglionic neurons and its consequences during, immediately following and several months after treatment"[http://vir.sgmjournals.org/cgi/content/full/81/10/2385]"</ref><ref>Famciclovir and Valaciclovir Differ in the Prevention of Herpes Simplex Virus Type 1 Latency in Mice: a Quantitative Study"[http://aac.asm.org/cgi/content/full/42/7/1555]"</ref><ref>Persistence of Infectious Herpes Simplex Virus Type 2 in the Nervous System in Mice after Antiviral Chemotherapy"[http://aac.asm.org/cgi/content/full/44/1/97]"</ref> A review of human subjects treated for five days with famciclovir 250&nbsp;mg three times daily during their first herpes episode found that only 4.2 percent experienced a recurrence within six months after the first outbreak, a fivefold decrease compared to the 19 percent recurrence in acyclovir-treated patients.<ref>Observation May Indicate A Possible Clinical Effect On Latency"[http://www.pslgroup.com/dg/D29E.htm]"</ref> Despite these promising results, early famciclovir treatment for herpes in this or similar dosage regimes has yet to find mainstream adoption. As a result, some doctors and patients have opted for [[off-label use]]. One suggested regime is famciclovir at 10–20&nbsp;mg/kg per day for 5–10 days, with treatment to commence as soon as possible after the first herpes infection (not the first symptoms or outbreak), and the most effective time for initiating treatment to be five days or less after the first herpes infection. However, the window of opportunity for this treatment is only a few months after first infection with the virus, following this the potential effect on latency drops to zero.<ref name=Thackray>{{cite journal
| author=Thackray AM, Field HJ.
| title=Differential effects of famciclovir and valaciclovir on the pathogenesis of herpes simplex virus in a murine infection model including reactivation from latency
| journal=J. Infect. Dis.
| year=1996
| pages=291–299
| volume=173
| issue=2
| pmid=8568288}}</ref>

Antiviral medications are also available as topical creams for treating recurrent outbreaks on the lips, although their effectiveness is disputed.<ref name="pmid8664786">{{cite journal
|author=Worrall G
|title=Evidence for efficacy of topical acyclovir in recurrent herpes labialis is weak
|journal=BMJ
|volume=313
|issue=7048
|page=46
|date= July 6, 1996 |pmid=8664786
|url=http://www.bmj.com/cgi/content/full/313/7048/46/a
}}</ref>
Penciclovir cream has a 7-17 hour longer cellular [[biological half-life|half-life]] than aciclovir cream, increasing its effectiveness relative to aciclovir when topically applied.<ref name="pmid9134943">{{cite journal
|author=Spruance SL, Rea TL, Thoming C, Tucker R, Saltzman R, Boon R
|title=Penciclovir cream for the treatment of herpes simplex labialis. A randomized, multicenter, double-blind, placebo-controlled trial. Topical Penciclovir Collaborative Study Group
|journal=JAMA
|volume=277
|issue=17
|pages=1374–9
|year=1997
|pmid=9134943
|url=http://jama.ama-assn.org/cgi/content/abstract/277/17/1374
|doi=10.1001/jama.277.17.1374}}</ref>

===Topical treatments===
[[Docosanol]], used in many cosmetics as an emollient and barrier ingredient, is also available as an over-the-counter (OTC) drug formula for the treatment of oral herpes simplex outbreaks. It was thought to prevent HSV from fusing to cell membranes, but this has not been proven and it is known that docosanol also enters the cytoplasm of cells. The OTC drug formulation of docosanol is marketed by Avanir Pharmaceuticals under the name Abreva. Abreva was approved for use after clinical trials by the FDA in July 2000.<ref>{{cite web
| title = Drug Name: ABREVA (docosanol) - approval
| publisher = centerwatch.com
| month = July | year = 2000
| url = http://www.centerwatch.com/patient/drugs/dru627.html
| accessdate = 2007-10-17 }}</ref>
Abreva was the first [[over-the-counter drug|over-the-counter]] [[antiviral drug]] approved for sale in the United States and Canada. Research leading to the licensing of Abreva showed that the OTC formula shortened recovery time to a moderate degree. Avanir Pharmaceuticals and GlaxoSmithKline Consumer Healthcare were the subject of a U.S. nationwide class-action suit in [[March, 2007]] due to the misleading claim that it cut recovery times in half.<ref>{{cite web
| title = California Court Upholds Settlement Of Class Action Over Cold Sore Medicationl
| publisher = BNA Inc.
| month = July | year = 2000
| url = http://subscript.bna.com/SAMPLES/plp.nsf/85256269004a991e8525611300214487/29d5bb623a50fd25852572ad0074f772?OpenDocument
| accessdate = 2007-10-17 }}</ref>

There is some limited research that has shown that [[tea tree oil]] may have topical anti-viral activity, especially with the [[Herpes]] virus<ref>{{cite journal | author=Bishop, C.D. | title=Anti-viral Activity of the Essential Oil of Melaleuca alternifolia | journal=Journal of Essential Oil Research | pages=641–644| year=1995 }}</ref> Upon first feeling tingling or soreness in the area (i.e when one bites his or her lip), prior to any physical manifestation, apply tea tree oil constantly for several hours. If caught early enough a cold sore will not form.

===Other drugs===
[[Cimetidine]], a common component of [[heartburn]] medication, and [[probenecid]] have been shown to reduce the [[Clearance (medicine)|renal clearance]] of aciclovir.<ref name=debony>{{cite journal
| author=De Bony F, Tod M, Bidault R, On NT, Posner J, Rolan P.
| title=Multiple interactions of cimetidine and probenecid with valaciclovir and its metabolite acyclovir
| journal=Antimicrob. Agents Chemother.
| year=2002
| pages=458–463
| volume=46
| issue=2
| pmid=11796358
| doi=10.1128/AAC.46.2.458-463.2002}}</ref> These compounds also reduce the rate, but not the extent, at which valaciclovir is converted into aciclovir.

Limited evidence suggests that low dose [[aspirin]] (125&nbsp;mg daily) might be beneficial in patients with recurrent HSV infections. Aspirin (acetylsalicylic acid) is an [[non-steroidal anti-inflammatory drug]] which reduces the level of [[prostaglandin]]s—naturally occurring lipid compounds—that are essential in creating [[inflammation]].<ref name=Karadi>{{cite journal
| author=Karadi I, Karpati S, Romics L.
| title=Aspirin in the management of recurrent herpes simplex virus infection
| journal=Ann. Intern. Med.
| year=1998
| pages=696–697
| volume=128
| issue=8
| pmid=9537952}}</ref> A recent study in animals showed inhibition of thermal (heat) [[Stress (medicine)|stress]] induced [[viral shedding]] of HSV-1 in the eye by aspirin, and a possible benefit in reducing the frequency of recurrences.<ref name=Gebhardt>{{cite journal
| author=Gebhardt BM, Varnell ED, Kaufman HE.
| title=Acetylsalicylic acid reduces viral shedding induced by thermal stress
| journal=Curr. Eye Res.
| year=2004
| pages=119–125
| volume=29
| issue=2-3
| pmid=15512958
| doi=10.1080/02713680490504588 }}</ref>
Another treatment is the use of petroleum jelly.{{Citation needed|date=January 2010}} Healing of cold sores is sped by barring water or saliva from reaching the sore.

===Alternative treatments===
[[Image:Koeh-094.jpg|thumb|Many people seek benefits in natural products and dietary supplements for treatment of herpes]]

Certain dietary adjustments, [[dietary supplement]]s, and [[Complementary and alternative medicine|alternative remedies]] are believed to be beneficial in the treatment of herpes, either alone, or in conjunction with prescribed antiviral therapy. There is insufficient scientific and clinical evidence to support the effective use of many of these compounds to treat herpes in humans.<ref name="pmid16209859">{{cite journal
|author=Perfect MM, Bourne N, Ebel C, Rosenthal SL
|title=Use of complementary and alternative medicine for the treatment of genital herpes
|journal=Herpes
|volume=12
|issue=2
|pages=38–41
|year=2005
|pmid=16209859 }}</ref>

[[Lysine]] supplementation has been used for the [[prophylaxis]] and treatment of herpes simplex. Lysine shows greater effect against HSV-1 but may not be active against all virus variants. Dosage is critical with less than 1 gram (1000&nbsp;mg) per day ineffective and more than 8 grams (8000&nbsp;mg) gaining no additional benefit. Lysine is most effective if corn based products (which contain high amounts of [[Arginine]]) such as popcorn are avoided during an outbreak. Lysine treatment is somewhat body mass sensitive with higher dosage required for effective treatment as body mass increases. It should be taken as 3 or more doses in a 24 hour period and should be started when first outbreak symptoms, such as skin numbness or itching, are detected.<ref name=McCune>{{cite journal
| author=McCune MA, Perry HO, Muller SA, O'Fallon WM.
| title=Treatment of recurrent herpes simplex infections with L-lysine monohydrochloride
| journal=Cutis.
| year=2005
| pages=366–373
| volume=34
| issue=4
| pmid=6435961}}</ref><ref name=Griffith>{{cite journal
| author=Griffith RS, Walsh DE, Myrmel KH, Thompson RW, Behforooz A.
| title=Success of L-lysine therapy in frequently recurrent herpes simplex infection. Treatment and prophylaxis
| journal=Dermatologica.
| year=1987
| pages=183–190
| volume=175
| issue=4
| pmid=3115841}}</ref><ref name=Griffith2>{{cite journal
| author=Griffith RS, Norins AL, Kagan C.
| title=A multicentered study of lysine therapy in Herpes simplex infection
| journal=Dermatologica.
| year=1978
| pages=257–267
| volume=156
| issue=5
| pmid=640102}}</ref>
[[Aloe vera]], available as a cream or gel, makes an affected area heal faster and may prevent recurrences.<ref>{{cite journal
| author=Vogler BK and Ernst E.
| title=Aloe vera: a systematic review of its clinical effectiveness.
| journal=British Journal of General Practice
| volume=49
| pages=823–828
| url=http://www.jr2.ox.ac.uk/bandolier/booth/alternat/AT125.html}}</ref>
[[Lemon balm]] (Melissa officinalis) has antiviral activity against HSV-2 in cell culture and may reduce HSV symptoms in herpes infected people.<ref name=Allahverdiyev>{{cite journal
| author=Allahverdiyev A, Duran N, Ozguven M, Koltas S.
| title=Antiviral activity of the volatile oils of Melissa officinalis L. against Herpes simplex virus type-2.
| journal=Phytomedicine.
| year=2004
| pages=657–661
| volume=11
| issue=7-8
| pmid=15636181
| doi=10.1016/j.phymed.2003.07.014 }}</ref><ref name="pmid10589440">{{cite journal
|author=Koytchev R, Alken RG, Dundarov S
|title=Balm mint extract (Lo-701) for topical treatment of recurring herpes labialis
|journal=Phytomedicine
|volume=6
|issue=4
|pages=225–30
|year=1999
|pmid=10589440
|doi=}}</ref><ref name="pmid10589440" />
[[Carrageenan]]s—linear sulphated [[polysaccharide]]s extracted from red [[seaweed]]s—have been shown to have antiviral effects in HSV-infected cells and in mice.<ref name=Zacharopoulos>{{cite journal
| author=Zacharopoulos VR, Phillips DM.
| title=Vaginal formulations of carrageenan protect mice from herpes simplex virus infection
| journal=Clin. Diagn. Lab. Immunol.
| year=1997
| pages=465–468
| volume=4
| issue=4
| pmid=9220165}}</ref><ref name=Carlucci>{{cite journal
| author=Carlucci MJ, Scolaro LA, Damonte EB.
| title=Inhibitory action of natural carrageenans on Herpes simplex virus infection of mouse astrocytes
| journal=Chemotherapy
| year=1999
| pages=429–436
| volume=45
| issue=6
| pmid=10567773
| doi=10.1159/000007236 }}</ref>
There is conflicting evidence on a possible benefit from extracts from the plant [[echinacea]] in treating oral<ref name="pmid12357386">{{cite journal
|author=Binns SE, Hudson J, Merali S, Arnason JT
|title=Antiviral activity of characterized extracts from echinacea spp. (Heliantheae: Asteraceae) against herpes simplex virus (HSV-I)
|journal=Planta Med.
|volume=68
|issue=9
|pages=780–3
|year=2002
|pmid=12357386
|doi=10.1055/s-2002-34397}}</ref>, but not genital, herpes.<ref name="pmid11231867">{{cite journal
|author=Vonau B, Chard S, Mandalia S, Wilkinson D, Barton SE
|title=Does the extract of the plant Echinacea purpurea influence the clinical course of recurrent genital herpes?
|journal=Int J STD AIDS
|volume=12
|issue=3
|pages=154–8
|year=2001
|pmid=11231867
|doi=10.1258/0956462011916947 }}</ref>
[[Resveratrol]], a compound naturally produced by plants and a component of red wine, prevents HSV replication in cultured cells and reduces cutaneous HSV lesion formation in mice. It is not considered potent enough to be an effective treatment on its own.<ref name=Docherty99>
{{cite journal
| author=Docherty JJ, Fu MM, Stiffler BS, Limperos RJ, Pokabla CM, DeLucia AL.
| title=Resveratrol inhibition of herpes simplex virus replication
| journal=Antiviral Res.
| year=1999
| pages=145–155
| volume=43
| issue=3
| pmid=10551373
| doi=10.1016/S0166-3542(99)00042-X }}</ref><ref name=Docherty04>{{cite journal
| author=Docherty JJ, Smith JS, Fu MM, Stoner T, Booth T.
| title=Effect of topically applied resveratrol on cutaneous herpes simplex virus infections in hairless mice
| journal=Antiviral Res.
| year=2004
| pages=19–26
| volume=61
| issue=1
| pmid=14670590
| doi=10.1016/j.antiviral.2003.07.001}}</ref>

Extracts from [[garlic]] have shown antiviral activity against HSV in cell culture experiments, although the extremely high concentrations of the extracts required to produce an antiviral effect was also toxic to the cells.<ref name="pmid1470664">{{cite journal
|author=Weber ND, Andersen DO, North JA, Murray BK, Lawson LD, Hughes BG
|title=In vitro virucidal effects of Allium sativum (garlic) extract and compounds
|journal=Planta Med.
|volume=58
|issue=5
|pages=417–23
|year=1992
|pmid=1470664
|doi=10.1055/s-2006-961504 }}</ref>
The plant [[Prunella vulgaris]], commonly known as ''selfheal'', also prevents expression of both type 1 and type 2 herpes in cultured cells.<ref name=saritamackita> {{cite journal
| author=Chiu LC, Zhub W, Oo VE
| title=A polysaccharide fraction from medicinal herb Prunella vulgaris downregulates the expression of herpes simplex virus antigen in Vero cells
| journal=Journal of Ethnopharmacology
| year=2004
| pages=63–68
| volume=93
| issue=1
| doi=10.1016/j.jep.2004.03.024 }}</ref>

[[Lactoferrin]], a component of [[whey]] protein, has been shown to have a synergistic effect with aciclovir against HSV in vitro.<ref name=Andersen>
{{cite journal
| author=Andersen JH, Jenssen H, Gutteberg TJ.
| title=Lactoferrin and lactoferricin inhibit Herpes simplex 1 and 2 infection and exhibit synergy when combined with acyclovir
| journal=Antiviral Res.
| year=2003
| pages=209–215
| volume=58
| issue=3
| pmid=12767468
| doi=10.1016/S0166-3542(02)00214-0 }}</ref>

Some dietary supplements have been suggested to positively treat herpes. These include [[vitamin C]], [[vitamin A]], [[vitamin E]], and [[zinc]].<ref name="pmid16813459">{{cite journal
|author=Gaby AR
|title=Natural remedies for Herpes simplex
|journal=Altern Med Rev
|volume=11
|issue=2
|pages=93–101
|year=2006
|pmid=16813459 }}</ref><ref name="pmid16405618">{{cite journal
|author=Yazici AC, Baz K, Ikizoglu G
|title=Recurrent herpes labialis during isotretinoin therapy: is there a role for photosensitivity?
|journal=J Eur Acad Dermatol Venereol
|volume=20
|issue=1
|pages=93–5
|year=2006
|pmid=16405618
|doi=10.1111/j.1468-3083.2005.01358.x}}</ref>
[[Butylated hydroxytoluene]] (BHT), commonly available as a [[food preservative]], has been shown in cell culture and animal studies to inactivate herpes virus.<ref>{{cite journal
|author=Snipes W, Person S, Keith A, Cupp J |title=Butylated hydroxytoluene inactivated lipid-containing viruses |journal=Science |volume=188 |issue=4183 |pages=64–6 |year=1975 |month=April |pmid=163494 |url=http://www.sciencemag.org/cgi/pmidlookup?view=long&pmid=163494
|doi=10.1126/science.163494}}</ref><ref>{{cite journal |author=Richards JT, Katz ME, Kern ER |title=Topical butylated hydroxytoluene treatment of genital herpes simplex virus infections of guinea pigs |journal=Antiviral Res. |volume=5 |issue=5 |pages=281–90 |year=1985 |month=October |pmid=2998276 |url=http://linkinghub.elsevier.com/retrieve/pii/0166-3542(85)90042-7 |doi=10.1016/0166-3542(85)90042-7}}</ref> However, BHT has not been clinically tested and approved to treat herpes infections in humans.

==Prognosis==
Following active infection, herpes viruses establish a latent infection in sensory and autonomic [[ganglia]] of the nervous system. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of the [[cell nucleus|nucleus]] of a nerve's [[Soma (biology)|cell body]]. HSV latency is static—no virus is produced—and is controlled by a number of viral genes, including [[HHV LAT|Latency Associated Transcript]] (LAT).<ref name="pmid12409612">{{cite journal |author=Stumpf MP, Laidlaw Z, Jansen VA |title=Herpes viruses hedge their bets |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=99 |issue=23 |pages=15234–7 |year=2002 |pmid=12409612 |url=http://www.pnas.org/content/99/23/15234 |doi=10.1073/pnas.232546899}}</ref>

Many HSV-infected people experience recurrence within the first year of infection.<ref name="pmid18156035"/> [[Prodrome]] precedes development of lesions. Prodromal symptoms include tingling ([[paresthesia]]), itching, and pain where lumbosacral nerves innervate the skin. Prodrome may occur as long as several days or as short as a few hours before lesions develop. Beginning antiviral treatment when prodrome is experienced can reduce the appearance and duration of lesions in some individuals. During recurrence, fewer lesions are likely to develop, lesions are less painful and heal faster (within 5–10 days without antiviral treatment) than those occurring during the primary infection.<ref name="pmid18156035"/> Subsequent outbreaks tend to be periodic or episodic, occurring on average four to five times a year when not using antiviral therapy.

The causes of reactivation are uncertain, but several potential triggers have been documented. A recent study (2009) showed that a protein [[VP16]] plays a key role in reactivation of the dormant virus.<ref> http://www.sciencenews.org/view/generic/id/42223/title/How_herpes_re-rears_its_ugly_head_</ref><!--PMID: 19321615 and PMID: 19325890 possible sources, --> Changes in the immune system during [[menstruation]] may play a role in HSV-1 reactivation.<ref name="pmid11022124">{{cite journal |author=Myśliwska J, Trzonkowski P, Bryl E, Lukaszuk K, Myśliwski A |title=Lower interleukin-2 and higher serum tumor necrosis factor-a levels are associated with perimenstrual, recurrent, facial Herpes simplex infection in young women |journal=Eur. Cytokine Netw. |volume=11 |issue=3 |pages=397–406 |year=2000 |pmid=11022124 |doi=}}</ref><ref name="pmid4526372">{{cite journal |author=Segal AL, Katcher AH, Brightman VJ, Miller MF |title=Recurrent herpes labialis, recurrent aphthous ulcers, and the menstrual cycle |journal=J. Dent. Res. |volume=53 |issue=4 |pages=797–803 |year=1974 |pmid=4526372 |doi=}}</ref> Concurrent infections, such as viral [[upper respiratory tract infection]] or other febrile diseases, can cause outbreaks. Reactivation due to infection is the likely source of the historic terms ''cold sore'' and ''fever blister''.

Other identified triggers include: local injury to the face, lips, eyes, or mouth, trauma, surgery, [[radiotherapy]], and exposure to wind, [[ultraviolet light]], or sunlight.<ref name="pmid18083428">{{cite journal |author=Chambers A, Perry M |title=Salivary mediated autoinoculation of herpes simplex virus on the face in the absence of "cold sores," after trauma |journal=J. Oral Maxillofac. Surg. |volume=66 |issue=1 |pages=136–8 |year=2008 |pmid=18083428 |doi=10.1016/j.joms.2006.07.019}}</ref><ref name="pmid2821086">{{cite journal |author=Perna JJ, Mannix ML, Rooney JF, Notkins AL, Straus SE |title=Reactivation of latent herpes simplex virus infection by ultraviolet light: a human model |journal=J. Am. Acad. Dermatol. |volume=17 |issue=3 |pages=473–8 |year=1987 |pmid=2821086 |doi=10.1016/S0190-9622(87)70232-1}}</ref><ref name="pmid1323616">{{cite journal |author=Rooney JF, Straus SE, Mannix ML, ''et al.'' |title=UV light-induced reactivation of herpes simplex virus type 2 and prevention by acyclovir |journal=J. Infect. Dis. |volume=166 |issue=3 |pages=500–6 |year=1992 |pmid=1323616 |doi=}}</ref><ref name="pmid9377190">{{cite journal |author=Oakley C, Epstein JB, Sherlock CH |title=Reactivation of oral herpes simplex virus: implications for clinical management of herpes simplex virus recurrence during radiotherapy |journal=Oral Surg Oral Med Oral Pathol Oral Radiol Endod |volume=84 |issue=3 |pages=272–8 |year=1997 |pmid=9377190 |doi=10.1016/S1079-2104(97)90342-5}}</ref><ref name="pmid15603217">{{cite journal |author=Ichihashi M, Nagai H, Matsunaga K |title=Sunlight is an important causative factor of recurrent herpes simplex |journal=Cutis |volume=74 |issue=5 Suppl |pages=14–8 |year=2004 |pmid=15603217 |doi=}}</ref>

The frequency and severity of recurrent outbreaks vary greatly between patients. Some individuals' outbreaks can be quite debilitating with large, painful lesions persisting for several weeks, while others will experience only minor itching or burning for a few days. An immunity to the virus is built over time. Most infected individuals will experience fewer outbreaks and outbreak symptoms will often become less severe. After several years, some people will become perpetually [[asymptomatic]] and will no longer experience outbreaks, though they may still be contagious to others. Immuno-compromised individuals may experience episodes that are longer, more frequent, and more severe. Antiviral medication has been proven to shorten the frequency and duration of outbreaks.<ref name="pmid18192785">{{cite journal |author=Martinez V, Caumes E, Chosidow O |title=Treatment to prevent recurrent genital herpes |journal=Curr Opin Infect Dis |volume=21 |issue=1 |pages=42–48 |year=2008 |pmid=18192785 |doi=10.1097/QCO.0b013e3282f3d9d3}}</ref> Outbreaks may occur at the original site of the infection or in proximity to nerve endings that reach out from the infected ganglia. In the case of a genital infection, sores can appear at the original site of infection or near the base of the spine, the buttocks, or the back of the thighs.

==History==
Herpes has been known for at least 2,000 years. It is said that Emperor [[Tiberius]] banned kissing in Rome for a time due to so many people having cold sores. In the 16th century ''[[Romeo and Juliet]]'', it is mentioned that there are blisters in "o'er ladies' lips." In 18th century it was so common among prostitutes that it was called "a vocational disease of women."<ref name=scarlet />

Herpes was not found to be a virus until the 1940s.<ref name=scarlet />

Herpes antiviral therapy began in the early 1960s with the experimental use of medication that interfered with viral replication called [[deoxyribonucleic acid]] (DNA) inhibitors. The original use was against normally fatal or disabilitating illness such as adult encephalitis,<ref name="pmid4790599">{{cite journal
|author=Chow AW, Roland A, Fiala M, ''et al.''
|title=Cytosine arabinoside therapy for herpes simplex encephalitis--clinical experience with six patients
|journal=Antimicrob. Agents Chemother.
|volume=3
|issue=3
|pages=412–7
|year=1973
|month=March
|pmid=4790599
|pmc=444424
|doi=
|url=http://aac.asm.org/cgi/pmidlookup?view=long&pmid=4790599
}}</ref> keratitis,<ref name="pmid14454441">{{cite journal
|author=Kaufman HE, Howard GM
|title=Therapy of experimental herpes simplex keratitis
|journal=Invest Ophthalmol
|volume=1
|issue=
|pages=561–4
|year=1962
|month=August
|pmid=14454441
|doi=
|url=http://www.iovs.org/cgi/pmidlookup?view=long&pmid=14454441
}}</ref> in immunocompromised (transplant) patients,<ref name="pmid180198">{{cite journal
|author=Ch'ien LT, Whitley RJ, Alford CA, Galasso GJ
|title=Adenine arabinoside for therapy of herpes zoster in immunosuppressed patients: preliminary results of a collaborative study
|journal=J. Infect. Dis.
|volume=133 Suppl
|issue=
|pages=A184–91
|year=1976
|month=June
|pmid=180198
|doi=
|url=
}}</ref> or disseminated herpes zoster.<ref name="pmid5352659">{{cite journal
|author=McKelvey EM, Kwaan HC
|title=Cytosine arabinoside therapy for disseminated herpes zoster in a patient with IgG pyroglobulinemia
|journal=Blood
|volume=34
|issue=5
|pages=706–11
|year=1969
|month=November
|pmid=5352659
|doi=
|url=http://www.bloodjournal.org/cgi/pmidlookup?view=long&pmid=5352659
}}</ref> The original compounds used were 5-iodo-2'-deoxyuridine, AKA idoxuridine, IUdR, or(IDU) and 1-β-D-arabinofuranosylcytosine or ara-C,<ref name="pmid4364937">{{cite journal
|author=Fiala M, Chow A, Guze LB
|title=Susceptibility of herpesviruses to cytosine arabinoside: standardization of susceptibility test procedure and relative resistance of herpes simplex type 2 strains
|journal=Antimicrob. Agents Chemother.
|volume=1
|issue=4
|pages=354–7
|year=1972
|month=April
|pmid=4364937
|pmc=444221
|doi=
|url=http://aac.asm.org/cgi/pmidlookup?view=long&pmid=4364937
}}</ref> later marketed under the name cytosar or cytorabine. The usage expanded to include topical treatment of herpes simplex,<ref name="pmid6598">{{cite journal
|author=Allen LB, Hintz OJ, Wolf SM, ''et al.''
|title=Effect of 9-beta-D-arabinofuranosylhypoxanthine 5'-monophosphate on genital lesions and encephalitis induced by Herpesvirus hominis type 2 in female mice
|journal=J. Infect. Dis.
|volume=133 Suppl
|issue=
|pages=A178–83
|year=1976
|month=June
|pmid=6598
|doi=
|url=
}}</ref> zoster, and varicella.<ref name="pmid4190397">{{cite journal
|author=Juel-Jensen BE
|title=Varicella and cytosine arabinoside
|journal=Lancet
|volume=1
|issue=7646
|page=572
|year=1970
|month=March
|pmid=4190397
|doi=10.1016/S0140-6736(70)90815-9
|url=
}}</ref> Some trials combined different antivirals with differing results.<ref name="pmid4790599"/> The introduction of 9-β-D-arabinofuranosyladenine, AKA ara-A or vidarabine, considerably less toxic than Ara-C, in the mid 1970s, heralded the way for the beginning of regular neonatal antiviral treatment. Vidarabine was the first systemically administered antiviral medication with activity against HSV for which therapeutic efficacy outweighed toxicity for the management of life-threatening HSV disease. Intravenous vidarabine was licensed for use by the [[U.S. Food and Drug Administration]] (FDA) in 1977. Other experimental antivirals of that period included: Heparin <ref name="pmid4289440">{{cite journal
|author=Nahmias AJ, Kibrick S
|title=Inhibitory effect of heparin on herpes simplex virus
|journal=J. Bacteriol.
|volume=87
|issue=5
|pages=1060–6
|year=1964
|month=May
|pmid=4289440
|pmc=277146
|doi=
|url=http://jb.asm.org/cgi/pmidlookup?view=long&pmid=4289440
}}</ref>,
trifluorothymidine (TFT)<ref name="pmid4790562">{{cite journal
|author=Allen LB, Sidwell RW
|title=Target-organ treatment of neurotropic virus diseases: efficacy as a chemotherapy tool and comparison of activity of adenine arabinoside, cytosine arabinoside, idoxuridine, and trifluorothymidine
|journal=Antimicrob. Agents Chemother.
|volume=2
|issue=3
|pages=229–33
|year=1972
|month=September
|pmid=4790562
|pmc=444296
|doi=
|url=http://aac.asm.org/cgi/pmidlookup?view=long&pmid=4790562
}}</ref>, Ribivarin,<ref name="pmid212976">{{cite journal
|author=Allen LB, Wolf SM, Hintz CJ, Huffman JH, Sidwell RW
|title=Effect of ribavirin on Type 2 Herpesvirus hominis (HVH/2) in vitro and in vivo
|journal=Ann. N. Y. Acad. Sci.
|volume=284
|issue=
|pages=247–53
|year=1977
|month=March
|pmid=212976
|doi=10.1111/j.1749-6632.1977.tb21957.x
|url=
}}</ref> interferon,<ref name="pmid4404669">{{cite journal
|author=Allen LB, Cochran KW
|title=Target-organ treatment of neurotropic virus disease with interferon inducers
|journal=Infect. Immun.
|volume=6
|issue=5
|pages=819–23
|year=1972
|month=November
|pmid=4404669
|pmc=422616
|doi=
|url=http://iai.asm.org/cgi/pmidlookup?view=long&pmid=4404669
}}</ref> Virazole,<ref name="pmid4340949">{{cite journal
|author=Sidwell RW, Huffman JH, Khare GP, Allen LB, Witkowski JT, Robins RK
|title=Broad-spectrum antiviral activity of Virazole: 1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide
|journal=Science (journal)
|volume=177
|issue=50
|pages=705–6
|year=1972
|month=August
|pmid=4340949
|doi=
|url=http://www.sciencemag.org/cgi/pmidlookup?view=long&pmid=4340949
}}</ref> and 5-methoxymethyl-2'-deoxyuridine (MMUdR).<ref name="pmid1239978">{{cite journal
|author=Babiuk LA, Meldrum B, Gupta VS, Rouse BT
|title=Comparison of the antiviral effects of 5-methoxymethyl-deoxyuridine with 5-iododeoxyuridine, cytosine arabinoside, and adenine arabinoside
|journal=Antimicrob. Agents Chemother.
|volume=8
|issue=6
|pages=643–50
|year=1975
|month=December
|pmid=1239978
|pmc=429441
|doi=
|url=http://aac.asm.org/cgi/pmidlookup?view=long&pmid=1239978
}}</ref> The introduction of 9-(2-hydroxyethoxymethyl)guanine, AKA acyclovir, in the late 1970s<ref name="pmid91931">{{cite journal
|author=O'Meara A, Deasy PF, Hillary IB, Bridgen WD
|title=Acyclovir for treatment of mucocutaneous herpes infection in a child with leukaemia
|journal=Lancet
|volume=2
|issue=8153
|page=1196
|year=1979
|month=December
|pmid=91931
|doi=10.1016/S0140-6736(79)92428-0
|url=
}}</ref> raised antiviral treatment another notch and led to vidarabine vs. acyclovir trials in the late 1980s.<ref name="pmid1988829">{{cite journal
|author=Whitley R, Arvin A, Prober C, ''et al.''
|title=A controlled trial comparing vidarabine with acyclovir in neonatal herpes simplex virus infection. Infectious Diseases Collaborative Antiviral Study Group
|journal=N. Engl. J. Med.
|volume=324
|issue=7
|pages=444–9
|year=1991
|month=February
|pmid=1988829
|doi=
|url=http://content.nejm.org/cgi/content/abstract/324/7/444
}}</ref> The lower toxicity and ease of administration over vidarabine has led to acyclovir becoming the drug of choice for herpes treatment after it was licensed by the FDA in 1998.<ref name="pmid11483782">{{cite journal
|author=Kimberlin DW, Lin CY, Jacobs RF, ''et al.''
|title=Safety and efficacy of high-dose intravenous acyclovir in the management of neonatal herpes simplex virus infections
|journal=Pediatrics
|volume=108
|issue=2
|pages=230–8
|year=2001
|month=August
|pmid=11483782
|doi=10.1542/peds.108.2.230
|url=http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=11483782
}}</ref> Another advantage in the treatment of neonatal herpes included greater reductions in mortality and morbidity with increased dosages, something that did not occur when compared with increased dosages of vidarabine.<ref name="pmid11483782"/> On the other side of the equation, acyclovir seems to inhibit antibody response and newborns on acyclovir antiviral treatment experienced a slower rise in antibody titer than those on vidarabine.<ref name="pmid11483782"/>

==Society and culture==
Some people experience negative feelings related to the condition following diagnosis, particularly if they have acquired the genital form of the disease. Feelings can include [[depression]], fear of rejection, feelings of [[isolation]], fear of being found out, self-destructive feelings, and fear of masturbation.<ref name=Vezina>{{cite journal
| author=Vezina C, Steben M.
| title=Genital Herpes: Psychosexual Impacts and Counselling
| journal=The Canadian Journal of CME
| year=2001
| pages=125–34
| issue=June
| url=http://www.stacommunications.com/journals/cme/images/cmepdf/june01/hsv.pdf|format=PDF}}</ref> These feelings usually lessen over time. Much of the hysteria and stigma surrounding herpes stems from a media campaign beginning in the late 1970s and peaking in the early 1980s. There were multiple articles worded in fear-mongering and anxiety-provoking terminology, such as the now ubiquitous "attacks," "outbreaks," "victims," and "sufferers." At one point the term "herpetic" even entered the popular lexicon. The articles were published by ''Reader's Digest'', ''U.S. News'', and ''Time'' magazine, among others. A made-for-TV movie was named ''Intimate Agony.'' The peak was when ''Time'' magazine had 'Herpes: The New Scarlet Letter' on the cover in August 1982, forever stigmatizing the word in the public mind.<ref name=scarlet>{{cite news |title= The New Scarlet Letter |work= [[Time (magazine)|Time]] |author= John Leo |date= 1982-08-02 |url= http://www.time.com/time/magazine/article/0,9171,1715020,00.html}}</ref> The scientific reality is that most people are asymptomatic, the virus causes no real health problems for a vast majority of people, and a vast majority of the Earth's population carries HSV-1, 2, or both. [[Herpes support groups]] have been formed in the United States and the UK, providing information about herpes and running message forums and dating websites for "sufferers."<ref>Lists of support groups and events:
* {{cite web
|url=http://www.herpesaz.com/html/groups.html
|title=A to Z Herpes Support Groups }}
* {{cite web
|url=http://www.herpes-coldsores.com/support/herpes.htm
|title=Herpes Support Groups }}
* {{cite web
|url=http://www.NationalHClub.com
|title=NationalHClub.com Local and National Herpes Events }}
</ref>

People with the herpes virus are often hesitant to divulge to other people, including friends and family, that they are infected. This is especially true of new or potential sexual partners whom they consider casual.<ref name=Green>{{cite journal
| author=Green J, Ferrier S, Kocsis A, Shadrick J, Ukoumunne OC, Murphy S, Hetherton J.
| title=Determinants of disclosure of genital herpes to partners.
| journal=Sex. Transm. Infect.
| year=2003
| pages=42–44
| volume=79
| issue=1
| pmid=12576613
| url=http://sti.bmj.com/cgi/content/full/79/1/42
| doi=10.1136/sti.79.1.42}}</ref> A perceived reaction is sometimes taken into account before making a decision about whether to inform new partners and at what point in the relationship. Many people choose not to disclose herpes status when first beginning to date a person, but wait until it becomes clear that the couple are moving towards a sexual relationship. Other people disclose herpes status at the beginning. Still others choose only to date other people who already have herpes. The premise of informing was constructed in conjunction with the emotional media coverage of the 1970s-1980s. Those infected prior to the mid- to late-1970s had never heard of informing the uninfected, or felt any need to inform. People who are not infected generally agree it is a responsible thing to do from a health perspective, since individuals who are not infected prefer to continue that way. With more knowledge about a partner, an individual can make an informed decision about a health issue.

==Research==
The [[National Institutes of Health]] (NIH) in the [[United States]] is conducting [[Clinical trial|phase III trials]] of [[Herpevac]], a vaccine against HSV-2.<ref name="titleHerpevac Trial for Women">{{cite web
|url=http://www.niaid.nih.gov/dmid/stds/herpevac/
|title=Herpevac Trial for Women |accessdate=2008-02-25}}</ref>
The vaccine has only been shown to be effective for women who have never been exposed to HSV-1. Overall, the vaccine is approximately 48% effective in preventing HSV-2 seropositivity and about 78% effective in preventing symptomatic HSV-2.<ref name="titleHerpevac Trial for Women">{{cite web |url=http://www.niaid.nih.gov/dmid/stds/herpevac/studyover_faqs.htm
|title=Herpevac Trial for Women
|accessdate=2008-03-04 }}</ref> During initial trials, the vaccine did not exhibit any evidence of preventing HSV-2 in males.<ref name="titleHerpevac Trial for Women"/> Additionally, the vaccine only reduced the acquisition of HSV-2 and symptoms due to newly acquired HSV-2 among women who did not have HSV-2 infection at the time they got the vaccine.<ref name="titleHerpevac Trial for Women"/> Because about 20% of persons in the United States have HSV-2 infection, this further reduces the population for whom this vaccine might be appropriate.<ref name="titleHerpevac Trial for Women"/>

Researchers at the [[University of Florida]] have made a hammerhead [[ribozyme]] that targets and cleaves the mRNA of essential genes in HSV-1. The hammerhead which targets the mRNA of the UL20 gene greatly reduced the level of HSV-1 ocular infection in rabbits and reduced the viral yield in vivo.<ref>{{cite web
|url=http://www.nature.com/mt/journal/v13/n1s/abs/mt2006942a.html
|title=Molecular Therapy - Abstract of article: 801. RNA Gene Therapy Targeting Herpes Simplex Virus }}</ref>The gene-targeting approach uses a specially designed RNA enzyme to inhibit strains of the herpes simplex virus. The enzyme disables a gene responsible for producing a protein involved in the maturation and release of viral particles in an infected cell. The technique appears to be effective in experiments with mice and rabbits, but further research is required before it can be attempted in people who are infected with herpes. <ref>{{cite web
|url=http://news.ufl.edu/2009/02/03/herpes-2/
|title=Potential new herpes therapy studied}}</ref>

More importantly, a breakthrough was made by [[Harvard Medical School]]'s Higgins Professor of [[Microbiology]], Professor David Knipe. His laboratory developed dl5-29, a replication-defective mutant virus that has proved successful both in preventing HSV-2/HSV-1 infections, and in combating the virus in already infected hosts, in animal models. Specifically, Knipe's lab has already shown that the replication-defective vaccine induces strong HSV-2-specific antibody and T-cell responses; protects against challenge with a wild-type HSV-2 virus; greatly reduces the severity of recurrent disease; provides cross-protection against HSV-1, and renders the virus unable to revert to a virulent state or to become latent.<ref>http://www.acambis.com/default.asp-id=2052.htm</ref> His vaccine is now being researched and developed by Accambis, and is due to be applied as an Investigational New Drug in 2009.<ref>http://focus.hms.harvard.edu/2008/030708/licensing.shtml</ref>

Another possibility to eradicate the HSV-1 variant is being pursued by Professor Bryan Cullen and his team at [[Duke University]]. By figuring out how to switch all copies of the virus in the host from [[latency]] to their active stage at the same time, rather than the way the virus copies normally stagger their activity stage, leaving some dormant somewhere at all times, it is thought that conventional anti-viral drugs can kill the entire virus population completely, since they can no longer hide in the nerve cells. One class of drugs called [[antagomir]] could serve this purpose. These are chemically engineered oligonucleotides or short segments of RNA, that can be made to mirror their target genetic material, namely herpes microRNAs. They could be engineered to attach and thus 'silence' the microRNA, thus rendering the virus incapable to keep latent in their host.<ref>http://www.reuters.com/article/healthNews/idUSN0229815620080702?pageNumber=2&virtualBrandChannel=0</ref> Professor Cullen believes a drug could be developed to block the microRNA whose job it is to suppress HSV-1 into latency.<ref>http://www.time.com/time/health/article/0,8599,1819739,00.html</ref>

Additionally, another solution may be found with regards to curing the infection. A cross anti-viral drug called [[Bavituximab]] has already proved successful in effectively treating mice and guinea pigs infected with various enveloped viruses. Herpes viruses fall within this category, and it is thought that the virus might be eradicated from the body using this drug.<ref>http://herpesisnormal.com/</ref> The drug works by binding onto infected cells, including cancer cells, and signaling to the immune system to come and destroy the problem cells. This is a novel technique in medicine and is eagerly anticipated. It is believed that cross-protection against latent viruses such as herpes simplex, Epstein-Barr, etc., will make an important contribution to improving public health.<ref>http://www.reuters.com/article/pressRelease/idUS203868+04-Nov-2009+PRN20091104 "Release"], Reuters</ref>

Vironova AB, which is a privately held Swedish biotech company, created an antiviral approach to stop viral growth by inhibiting viral structures from forming, e.g. the capsid. Correct assembly of structural proteins is essential for the virus to survive the extracellular environment and to become infectious, and is thus a suitable drug target. Vironova AB is dedicated to the development of antiviral therapeutics and virus diagnostics products to combat and prevent the spread of viral diseases.<ref>http://www.vironova.com/webpage.aspx?id=149</ref>

== See also ==
* [[List of cutaneous conditions]]

==References==
{{reflist|colwidth=30em}}

==External links==
<!--BEFORE inserting new links here you should first post it to the talk page, otherwise your edit is likely to be reverted-->

'''General'''
*[http://cdc.gov/std/Herpes/STDFact-Herpes.htm Genital Herpes Fact Sheet] at [[The Centers for Disease Control and Prevention]]
*"[http://www.fda.gov/fdac/features/2002/202_herp.html Genital Herpes: A Hidden Epidemic]" at [[U.S. Food and Drug Administration]]
*[http://www.information-on-herpes.com Herpes: A lay persons resource with information on symptoms and pictures.]

'''Images'''
*[http://www.lib.uiowa.edu/hardin/md/herpespictures.html Links to genital herpes pictures] (Hardin MD/[[University of Iowa]])
*[http://dermnet.com/moduleSearch.cfm?searchterm=herpes Herpes photo library at Dermnet]
*[http://www.skinsight.com/adult/orofacialHerpesSimplexVirusHSV.htm Pictures of Orofacial Herpes (Coldsores)] (Skinsight)
*[http://www.skinsight.com/adult/genitalHerpesSimplexVirusHSV.htm Clinical Pictures of Genital Herpes] (Skinsight)
*[http://webeye.ophth.uiowa.edu/eyeforum/atlassearch1.htm Atlas of Ophthalmology] (UoIowa), annotations under "herpes simplex"
*[http://yourstdhelp.com/herpes.html Herpes Pictures in Men and Women]

'''Other'''
<!--BEFORE inserting new links here you should first post it to the talk page, otherwise your edit is likely to be reverted.-->
*[http://www.askthestdexperts.com/ Ask the experts about herpes signs and symptoms]
*[http://www.ashastd.org/pdfs/blood_test.pdf Herpes Blood Tests Quick Reference Guide]
*[http://westoverheights.com/genital_herpes/handbook.html Updated Herpes Handbook from Westover Heights Clinic]
*"[http://www.medscape.com/viewarticle/489964 The Importance and Practicalities of Patient Counseling in the Prevention and Management of Genital Herpes]" (2004) at [[Medscape]]
*[http://www.ihmf.org/default.asp International Herpes Management Forum]
*[http://herpes.com/Nutrition.shtml Provides Ratios of Lysine to Arginine in Common Foods]

{{Diseases of the skin and appendages by morphology}}
{{STD/STI}}
{{Viral diseases}}

{{DEFAULTSORT:Herpes Simplex}}
[[Category:Virus-related cutaneous conditions]]
[[Category:Conditions of the mucous membranes]]
[[Category:Herpes]]
[[Category:Sexually transmitted diseases and infections]]
[[Category:Viral diseases]]
[[Category:Biology of bipolar disorder]]

[[ar:هربس بسيط]]
[[ca:Herpes simple]]
[[cs:Jednoduchý opar]]
[[da:Herpes]]
[[de:Herpes simplex]]
[[es:Herpes simple]]
[[eo:Herpeto]]
[[eu:Herpes]]
[[fa:تب‌خال]]
[[fr:Herpès]]
[[ko:단순 포진]]
[[io:Herpeto]]
[[id:Herpes simpleks]]
[[it:Herpes]]
[[he:הרפס]]
[[ht:VÈS]]
[[lv:Herpess]]
[[ms:Herpes]]
[[nl:Genitale herpes]]
[[ja:性器ヘルペス]]
[[pl:Zakażenia opryszczkowe]]
[[pt:Herpes]]
[[ru:Герпес]]
[[sk:Jednoduchý opar]]
[[sr:Херпес]]
[[tl:Herpes]]
[[th:เริม]]
[[uk:Герпес]]
[[zh:單純疱疹病毒]]

Revision as of 04:10, 3 February 2010

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